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Pulmonary ThromboembolismPulmonary Thromboembolism
(PTE)(PTE)
Dr. Mohankumar ThekkinkattilDr. Mohankumar Thekkinkattil, MD,ABIM,DSc,DPPR,FCCP.FAARC,FNCCP,FIASM, MD,ABIM,DSc,DPPR,FCCP.FAARC,FNCCP,FIASM
HOD & Senior Consultant Pulmonologist,HOD & Senior Consultant Pulmonologist,
Sri Ramakrishna hospital ,Sri Ramakrishna hospital ,
Coimbatore.Coimbatore.
India.India.
email: drtmkcbe@gmail.comemail: drtmkcbe@gmail.com
An Elusive Diagnosis

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GoalsGoals
 Understand the historical context of pulmonary emboli
 Comprehend the pathophysiology and know some common
risk factors
 Be aware of the clinical features of PE and have a basic
understanding of various diagnostic tests
 Gain a therapeutic approach to the treatment of PE and
discuss a simplified method in the work-up of PE
 Attempt to dispel a few “myths”about pulmonary emboli

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PerspectivePerspective
 A Common disorder and potentially deadly
 650,000 cases occurring annually
 Highest incidence in hospitalized patients
 Autopsy reports suggest it is commonly “missed”
diagnosed

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PerspectivePerspective
 Presentation is often “atypical”
 Signs and symptoms are frequently vague and
nonspecific and rarely “classic”
 Untreated mortality rate of 20% - 30%,
plummets to 5% with timely intervention

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Historical ContextHistorical Context
 Pre-1930’s
 Heparin : Treatment till now!!!!!
 Eugine Robin article in 1997 (diagnosis)

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Historical ContextHistorical Context
 PIOPED (Prospective Investigation of
Pulmonary Embolism Diagnosis) 1990
 The Electronic Era, 2000 and Beyond…

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So What Do We Do ???So What Do We Do ???
Confusing for Physician
Do we under diagnose/over diagnose?
Why don’t we have a standardized method of
work up after all these years?

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PathophysiologyPathophysiology
Rudolph Virchow, 1858
Triad:
 Hypercoagulability
 Stasis to flow
 Vessel injury

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Risk FactorsRisk Factors
Hypercoagulability
Malignancy
Nonmalignant thrombophilia
Pregnancy
Postpartum status (<4wk)
Estrogen/ OCP’s
Genetic mutations (Factor V Leiden, Protein C & S deficiency, Factor
VIII, Prothrombin mutations, anti-thrombin III
deficiency)
Venous Statis
Bedrest > 24 hr
Recent cast or external fixator
Long-distance travel or prolong automobile travel
Venous Injury
Recent surgery requiring endotracheal intubation
Recent trauma (especially the lower extremities and pelvis)

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Clinical PresentationClinical Presentation
 The Classic Triad: (Hemoptysis, Dyspnea, Pleuritic
Pain)
 Not very common!
 Occurs in less than 20% of patients with documented PE
 Three Clinical Presentations
– Pulmonary Infarction
– Submassive Embolism
– Massive Embolism

11. ClassificationClassification
Subclinical
Submassive: normal BP, possible RV
hypokinesia or dilatation
Massive: affects BP, RV afterload, PA systolic
pressure

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Mythology of PEMythology of PE
 Myth
– “Patients with pulmonary embolism are short of
breath and have chest pain!”
Reality:
You can forget about making the diagnosis on
clinical grounds, but wait…don’t plan on completely
ruling it out either!

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Clinical FeaturesClinical Features
Symptoms in Patients with Angio Proven PTE
Symptom Percent
Dyspnea 84
Chest Pain, pleuritic 74
Anxiety 59
Cough 53
Hemoptysis 30
Sweating 27
Chest Pain, nonpleuritic 14
Syncope 13

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Clinical FeaturesClinical Features
Signs with Angiographically Proven PE
Sign Percent
Tachypnea > 20/min 92
Rales 58
Accentuated S2 53
Tachycardia >100/min 44
Fever > 37.8 43
Diaphoresis 36
S3 or S4 gallop 34
Thrombophebitis 32
Lower extremity edema 24

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Who do we work up?Who do we work up?
-- Pretest ProbabilityPretest Probability
Definition: “The probability of the target
disorder (PE) before a diagnostic test
result is known”.
Used to decide how to proceed with
diagnostic testing and final disposition
“Guess”
– This is really what it boils down to!

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Diagnostic TestDiagnostic Test
 Imaging Studies
– CXR
– V/Q Scans
– Spiral Chest CT
– Pulmonary Angiography
– Echocardiograpy
 Laboratory Analysis
– CBC, ESR, Hgb/Hct,
– D-Dimer
– ABG’s
 Ancillary Testing
– ECG
– Pulse Oximetry

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Diagnostic TestingDiagnostic Testing
- CXR’s- CXR’s
Chest X-Ray Myth:
“You have to do a chest x-ray so you can find
Hampton’s hump or a Westermark sign.”
Reality:
Most chest x-rays in patients with PE are
nonspecific and insensitive

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Diagnostic TestingDiagnostic Testing
-- CXR’sCXR’s
Chest radiograph findings in patient with
pulmonary embolism
Result Percent
Cardiomegaly 27%
Normal study 24%
Atelectasis 23%
Elevated Hemidiaphragm 20%
Pulmonary Artery Enlargement 19%
Pleural Effusion 18%
Parenchymal Pulmonary Infiltrate 17%

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Chest X-ray Eponyms of PEChest X-ray Eponyms of PE
 Westermark's sign
– A dilation of the pulmonary vessels proximal to the
embolism along with collapse of distal vessels,
sometimes with a sharp cutoff.
 Hampton’s Hump
– A triangular or rounded pleural-based infiltrate with
the apex toward the hilum, usually located adjacent to
the hilum.

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Radiographic EponymsRadiographic Eponyms
- Hampton’s Hump, Westermark’s Sign- Hampton’s Hump, Westermark’s Sign
Westermark’s
Sign
Hampton’s Hump

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Diagnostic TestingDiagnostic Testing
– ECG’s– ECG’s
 ECG
– Most Common Findings:
 Tachycardia or nonspecific ST/T-wave changes
– Acute Cor Pulmonale or right strain patterns
 Tall peaked T-waves in lead II (P Pulmonale)
 Right axis deviation
 RBBB
 S1-Q3-T3 (Occurs in only 20% of PE patients)

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Diagnostic TestingDiagnostic Testing
-- Pulse OximetryPulse Oximetry
 The Pulse Oximetry Myth:
– “ You must do a pulse oximetry reading, since
patients with pulmonary embolism are hypoxemic!”
 Reality:
– Most patients with a PE have a normal pulse
oximetry, and most patients with an abnormal pulse
oximetry will not have a PE.

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Diagnostic TestingDiagnostic Testing
- ABG’s- ABG’s
 The ABG/ A-a Gradient myth:
– “You must do an arterial blood gas and calculate the alveolar-
arterial gradient. Normal A-a gradient virtually rules out PE”.
 Reality:
– The A-a gradient is a better measure of gas exchange than the
pO2, but it is nonspecific and insensitive in ruling out PE.

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Diagnostic TestingDiagnostic Testing
Echocardiography
– Consider in every patient with a documented
pulmonary embolism
 ECG maybe helpful in demonstrating right heart
strain
– Early fibrinolysis can reduce mortality 50%!

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Ancillary TestAncillary Test
 WBC
– Poor sensitivity and nonspecific
 Can be as high as 20,000 in some patients
 Hgb/Hct
– PTE does not alter count but if extreme, consider
polycythemia, a known risk factor
 ESR
– Don’t get one, terrible test in regard to any predictive
value

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D-dimer TestD-dimer Test
 Fibrin split product
 Circulating half-life of 4-6 hours
 Quantitative test have 80-85% sensitivity, and 93-100% negative
predictive value
 False Positives:
Pregnant Patients Post-partum < 1 week
Malignancy Surgery within 1 week
Advanced age > 80 years Sepsis
Hemmorrhage CVA
AMI Collagen Vascular Diseases
Hepatic Impairment

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Diagnostic TestingDiagnostic Testing
 D-dimer
– Qualitative
 Bed side RBC agglutination test
– “SimpliRED D-dimer”
– Quantitative
 Enzyme linked immunosorbent asssay “Dimertest”
 Positive assay is > 500ng/ml
 VIDAS D-dimer, 2nd
generation ELISA test

28. Plasma D-dimer ELISAPlasma D-dimer ELISA
usefull diagnostic approach
Sensitive but nonspecific test for PE
High negative predictive value when
concentration is <500 ng/mL
Can help reduce frequency of pulmonary
angiography
Diagnostic strategy of V/Q scanning plus

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Ventilation/Perfusion ScanVentilation/Perfusion Scan
- “V/Q Scan”- “V/Q Scan”
 A common modality to image the lung and its
use still stems from the PIOPED study.
 Relatively noninvasive and sadly most often
nondiagnostic
 In many centers remains the initial test of choice
 Preferred test in pregnant patients
 50 mrem vs 800mrem (with spiral CT)

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V/Q ScanV/Q Scan
 Technique
 Interpretation
– Normal
– Low probability/”nondiagnostic” (most common)
– High Probability
 Simplified approached to the interpretation of results:
High probability  Treat for PE
Normal Scan  If low pre-test, you are done
Everything else  Pursue another study (CT, Angio)

31. VQ Scan
Perfusion VentilationMismatch

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Spiral (Helical) Chest CTSpiral (Helical) Chest CT
 Advantages
– Noninvasive and Rapid
– Alternative Diagnosis
 Disadvantages
– Costly
– Risk to patients with borderline renal function
– Hard to detect subsegmental pulmonary emboli

33. Spiral CT/ Multislice
Ascending Aorta
Lt Pulmonary Artery
Main Pulmonary Artery
Rt Pulmonary Artery
Descending Aorta
Thrombus

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Pulmonary AngiographyPulmonary Angiography
“Gold Standard”
– Performed in an Interventional Cath Lab
Positive result is a “cutoff” of flow or
intraluminal filling defect
“Court of Last Resort”

35. Pulmonary Angiogram

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Treatment:Treatment:
Goals:
 Prevent death from a current embolic event
 Reduce the likelihood of recurrent embolic
events
 Minimize the long-term morbidity of the event
Dr. T.M.K explaining
the CT results
Patient
replies:
“Uh-huh,
when do I
get to eat!”

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TreatmentTreatment
 Anticoagulants
– Heparin
 Provides immediate thrombin inhibition, which prevents
thrombus extension
 Does not dissolve existing clot
 Will not work in patients with antithrombin III def.
– In this case use hirudins
 Few absolute contraindications

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TreatmentTreatment
Anticoagulants
– Heparin
 Available as Unfractionated or LMW Heparin
– FDA approved dosing:
• Unfractionated: 80 units/kg bolus, 18 units/kg/Hr
• LMWH: 1 mg/kg Q 12 or 1.5mg/kg Q D
 LMWH preferred in pregnant patients

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TreatmentTreatment
 Anticoagulants
– Warfarin (Coumadin)
 Interferes with the action of Vit-K dependent factors: II, VII,
IX, and X, as well as protein C & S
 Causes temporary hypercoagulable state in first 5 days of
treatment
– Important a patient is anticoagulated with heparin before
initiating warfarin therapy
 Target INR is 2.5 – 3.0

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TreatmentTreatment
 Fibrinolytic Therapy (Alteplase)
– Indications:
 Documented PE with:
– Persistent hypotension
– Syncope with persistent hemodynamic compromise
– Significant hypoxemia
– +/- patient with acute right heart strain
 Approved regimen is 100mg as a continuous IV infusion
over 10 minutes for critically ill patients.

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TreatmentTreatment
Embolectomy
– Prefininolytic therapy this was only therapy
for massive PE
– Carries a 40% operative mortality
– Alternative is Transvenous Catheter
Embolectomy

42. TreatmentTreatment
Thrombolytic therapy
– Streptokinase
– Urokinase
– Altepase (t-PA)
 In haemodynamically unstable patients even with
heparin

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A Simplified AlgorithmA Simplified Algorithm
Pre-test probability
D-dimer
CT angiography
Low Pre-test, D-dimer (-),
patient had < 1.7% 90 day
PE occurrence in a Mayo
Clinic Study

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Special CircumstancesSpecial Circumstances
 Morbid Obesity
 Pregnancy
 V/Q has considerable less radiation
– 50 mrem vs. 800 mrem
 Almost all will have positive D-Dimer
 Heparin safe in pregnancy
 Witnessed Cardiac Arrest
 Standard ACLS, if known PE, the lytics.

45. Recommendations
Duration of therapy
 First thromboembolic event in the context of a reversible
risk factor
-- Treated for three to six months
 Idiopathic first thromboembolic event
-- AT LEAST full six months of treatment
-- Further therapy at discretion of clinician
 Recurrent venous thrombosis or a continuing risk factor --
Treated indefinitely.

46. Adverse events and clinicalAdverse events and clinical
outcomeoutcome
 Recurrent PE
 Death
 Bleeding Complications:
Intracranial bleed
 Pulmonary hypertension

47. Differential diagnosisDifferential diagnosis
 Pneumothorax
 Thoracic herpes zoster
 Rib fracture
 Musculoskeletal pain
 Primary or metastatic intrathoracic cancer
 Hyperventilation syndrome
 Infradiaphragmatic processes (e.g. Acute
cholecytitis)

48. Differential diagnosisDifferential diagnosis
Acute myocardial infarction
Pericarditis
Congestive heart failure
Pneumonia, pleuritis
Asthma
COPD

49. Prevention
• Heparin
• Low-molecular-weight heparin
• Graded compression stockings
Have been shown to reduce the incidence
of pulmonary embolism in hospitalized
patients.

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1. Which of the following is not a part of
virchows triad?
a) Hypercoagulability
b) Stasis to flow
c) Vessel injury
d) History of previous DVT

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2. Which of the following is the propper
treatment of fat emboli?
a) Platelets
b) High dose steroids
c) Heparin
d) cryoprecipitate

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3. The Classic Triad of patients presenting
to the ED with PE includes all of the
following except:
a) Hemoptysis
b) Dyspnea
c) + Homans’ sign
d) Pleuritic Pain

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4. What is the most common
symptom in a patient with Angio
Proven PTE?
a) Dyspnea
b) Chest Pain, pleuritic
c) Anxiety
d) Cough

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5. What is the most common ecg finding in
patients with PE?
a) Right axis deviation
b) RBBB
c) S1-Q3-T3
d) Tall peaked T-waves in lead II (P pulmonale)
e) Sinus tachycardia

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AnswersAnswers
1. D
2. B
3. C
4. A
5. E

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ConclusionConclusion
Summary PointsSummary Points
 Pulmonary Emboli remain a potentially deadly and common event whichPulmonary Emboli remain a potentially deadly and common event which
may present in various waysmay present in various ways
 Don't’ be fooled if your patient lacks the “classic” signs and symptoms!Don't’ be fooled if your patient lacks the “classic” signs and symptoms!
 Consider PE in any patient with an unexplainable cause of dyspnea,Consider PE in any patient with an unexplainable cause of dyspnea,
pleuritic chest pain, or findings of tachycardia, tachpnea, or hypoxemiapleuritic chest pain, or findings of tachycardia, tachpnea, or hypoxemia
 22ndnd
Generation Qualitative D-Dimers have NPV of 93-99%Generation Qualitative D-Dimers have NPV of 93-99%
 Heparin remains the mainstay of therapy with the initiation of WarfarinHeparin remains the mainstay of therapy with the initiation of Warfarin
to followto follow
 Simplified Algorithm: ( Pretest probability, D-Dimer, +/- CT angio), thenSimplified Algorithm: ( Pretest probability, D-Dimer, +/- CT angio), then
disposition)disposition)

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The End!The End!
Questions????